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Results for “ASPHYXIA”

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At least 19 recordsLinked to original sources
PubMed2000

Anticonvulsants for preventing mortality and morbidity in full term newborns with perinatal asphyxia.

OBJECTIVES: To assess the benefits and harm of administering anticonvulsants to infants of 37 weeks gestation or more following perinatal asphyxia with the primary aims of prevention of death or subsequent severe neurodevelopmental disability and/or the prevention of seizures. SEARCH STRATEGY: Relevant randomised controlled trials were identified using a combination of electronic database searches (MEDLINE), hand searches and a search of the Neonatal Review Group trials register. SELECTION CRITERIA: All randomised, or quasi-randomised, controlled clinical trials with reported data comparing the following outcomes: mortality, neurodevelopmental disability, neonatal seizures and adverse events, following anticonvulsant therapy in term infants (37 weeks or more), compared to controls with or without placebo, following perinatal asphyxia. DATA COLLECTION AND ANALYSIS: Methodological quality and validity of studies were assessed without consideration of the results. Data relevant to the outcome were extracted and analysed. MAIN RESULTS: Five randomised or quasi-randomised controlled trials which met the selection criteria were identified. No studies were of sufficient methodological quality and size to demonstrate a valid, clinically significant change in the risk of mortality or severe neurodevelopmental disability. A meta-analysis combining three studies comparing barbiturates with conventional therapy following perinatal asphyxia demonstrated no difference in risks of death, severe neurodevelopmental disability, or death or severe neurodevelopmental disability. REVIEWER'S CONCLUSIONS: At the present time, anticonvulsant therapy to term infants in the immediate period following perinatal asphyxia cannot be recommended for routine clinical practice, other than in the treatment of prolonged or frequent clinical seizures. Any future studies should be of high quality: randomised control trials with allocation concealment, performance and outcome assessment blinding. Such studies should be of sufficient size, with minimal attrition, to have the power to detect clinically important reductions in mortality and severe neurodevelopmental disability, as the primary outcome measures.

Anticonvulsants↗
PubMed2002

Chronic intermittent asphyxia impairs rat upper airway muscle responses to acute hypoxia and asphyxia.

BACKGROUND: Obstructive sleep apnea (OSA) is a major clinical disorder that is characterized by multiple episodes of upper airway obstruction due to the failure of the upper airway dilator muscles to maintain upper airway patency. This results in chronic intermittent asphyxia (CIA) due to repetitive apneas, but very little is known about the effects of CIA on upper airway muscle function. OBJECTIVE: To test the hypothesis that CIA affects upper airway muscle activity and electromyogram (EMG) responses to acute hypoxia and asphyxia. DESIGN: Record upper airway EMG responses to acute hypoxia and asphyxia in control and CIA-treated rats. SETTING: Department of Physiology, Royal College of Surgeons in Ireland, Dublin, Ireland. MEASUREMENTS: Sternohyoid (SH) muscle and diaphragm (DIA) muscle EMG activities were recorded in both groups during normoxia, hypoxia (7.5% O(2) in N(2)), and asphyxia (7.5% O(2) and 3% CO(2)) under pentobarbitone anesthesia. RESULTS: Baseline SH EMG activity was significantly elevated in the CIA-treated rats compared to the controls, whereas DIA EMG activity was similar in the two groups. In addition, CIA significantly reduced SH EMG but not DIA EMG responses to acute hypoxia and asphyxia. CONCLUSIONS: The elevated upper airway muscle activity associated with OSA in humans during wakefulness is due at least in part to CIA. We propose that a reduction in the response of upper airway dilator muscles to acute asphyxia following upper airway obstruction is likely to cause further asphyxic insult, leading to a vicious feed-forward cycle exacerbating the condition. Our results suggest that CIA contributes to the pathophysiology of sleep-disordered breathing.

Analysis of Variance↗
PubMed1999

[Neonatal asphyxia--prognosis based on clinical findings during delivery and the first day of life. A retrospective study of 54 newborn infants with asphyxia].

A retrospective study of a cohort of 54 term infants with perinatal asphyxia admitted to the neonatal intensive care unit at Hvidovre University Hospital i 1995 is described. The purpose of the study was to find clinical markers for prediction of outcome after perinatal asphyxia. Neither complications of pregnancy, gestational age, the sex of the infant, passage of meconium before delivery, abnormal fetal heart rate nor birth weight seemed to have any interrelationship with outcome. The Apgar score was more depressed, and the metabolic acidosis worse among the infants with poor outcome. The best predictor of outcome after intrapartum asphyxia was the severity of postasphyxial encephalopathy. No infant with mild or moderate postasphyxial encephalopathy died or developed any handicap. All with severe postasphyxial encephalopathy either died or developed minor handicaps.

Apgar Score↗
PubMed1998

Plasma platelet-activating factor levels in newborn infants with and without perinatal asphyxia: is it an additional marker of perinatal asphyxia?

BACKGROUND: Hypoxic-ischemic encephalopathy (HIE) is still a very important cause of neonatal mortality and morbidity. Recently platelet-activating factor (PAF) has been accused of being responsible for the neuronal damage in hypoxic-ischemic brain. METHODS: Therefore, we conducted a study in newborns with perinatal asphyxia to try to show the relationship between the clinical severity and plasma PAF levels. RESULTS: Mean plasma levels of 19 asphyxiated infants (997.8 +/- 363.5 pg/mL) were significantly higher than that of 20 healthy infants (410.2 +/- 148.6 pg/mL, P < 0.0001). Patients with clinically severe HIE had significantly higher levels of PAF (1494.2 +/- 386.6 pg/mL) when compared with patients with mild HIE (815 +/- 114.5 pg/mL) and with moderate HIE (828.3 +/- 61.1 pg/mL). There was a significant correlation between plasma PAF concentration and arterial pH and base deficit, but no correlation with platelet and leukocyte counts. CONCLUSIONS: Plasma PAF levels correlating with the severity of HIE is interpreted to mean that high PAF levels may be an indicator of clinical severity and probably the poorer prognosis of patients with HIE.

Apgar Score↗
PubMed1992

Studies on asphyxia: morphological research for the aid of diagnosis of asphyxia using light and electron microscopy and immunohistochemical methods.

The lattice-form structure and/or tubular myelin can be found in the debris-like structure which is the pinkish substance in the alveolar space in the Hematoxylin & Eosin stained sections. These findings were obtained by using rats in the air containing oxygen of 5% or mixing and/or contaminating each of methane, carbon dioxide, carbon monoxide and freon gases. The immunohistochemical detection using the monoclonal mouse antibody against human pulmonary surfactant (PS) apoprotein is of highly useful. The positive reaction products observed in the alveolar space indicate the localization of the tubular myelin. The data suggest that the PS appears when the inhaled air contains oxygen in low concentration. The immunohistochemical method using the antibody against human PS apoprotein is worth applying for the diagnosis of oxygen deficiency including the respiratory distress syndrome (RDS) of the new born. We conclude that the appearance of the positive reaction products suggests that, at least, the air did not come in contact with the surface of alveoli, which leads us to the diagnosis of death was from oxygen deficiency, even if we are at the stage when the mode of death is undetermined.

Animals↗